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Stimulation of acetylcholine receptors impairs host defence during pneumococcal pneumonia

¹ Center for Infection and Immunity Amsterdam (CINIMA), ² Center for Experimental and Molecular Medicine, and ³ Dept of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

CORRESPONDENCE: T. van der Poll, Academic Medical Center, Meibergdreef 9, Room G2-130, 1105 AZ Amsterdam, The Netherlands. Fax: 31 206977192. E-mail: t.vanderpoll{at}amc.uva.nl

Keywords: Airway infection, airway inflammation, animal, chemokines, cytokines

Received: July 7, 2008
Accepted September 19, 2008

The cholinergic nervous system can inhibit the systemic inflammation accompanying sepsis by virtue of a specific action of acetylcholine on 7 cholinergic receptors. The current authors sought to determine the effect of nicotine, an 7 cholinergic receptor agonist, on the host response to pneumonia caused by Streptococcus pneumoniae.

Mice were intranasally infected with S. pneumoniae and treated with nicotine or saline intraperitoneally using a treatment schedule shown to improve host defence against abdominal sepsis.

Nicotine treatment was associated with a transiently enhanced growth of S. pneumoniae, as indicated by higher bacterial loads in both lungs and blood at 24 h after infection. At 48 h after infection, bacterial burdens had increased in both treatment groups and differences were no longer present. Remarkably, mice treated with nicotine showed enhanced lung inflammation at 24 h after infection. Moreover, both lung and plasma concentrations of the pro-inflammatory cytokines tumour necrosis factor- and interferon- were higher in nicotine-treated animals at this time-point. Additional studies examining the effect of nicotine on the immediate (4-h) inflammatory response to S. pneumoniae did not reveal an anti-inflammatory effect of nicotine either.

The present data suggest that nicotine transiently impairs host defence in pneumococcal pneumonia.

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